Effects of Mg2+ on basal and beta‐adrenergic‐stimulated delayed rectifier potassium current in frog atrial myocytes.

1. The effects of internal Mg2+ ions on the delayed rectifier potassium current (IK) of bull‐frog atrial myocytes were studied using the whole‐cell configuration of the patch‐clamp technique with a perfusable patch electrode. 2. Initial variations in IK amplitude were dependent on [Mg2+]i. With [Mg2+] greater than 1 mM, the amplitude of IK usually decreased after initiating the whole‐cell recording configuration (run‐down); with [Mg2+]i less than 1 mM, IK usually increased (run‐up). Mg2+ blocked IK with an apparent half‐maximal effect of 0.6 mM [Mg2+]i. 3. The basal free [Mg2+]i, indicated by the amplitude of IK before run‐up or run‐down, was estimated from the relationship between [Mg2+]i and IK to be 0.8 mM. 4. The amplitude of both the activation curve and the instantaneous voltage‐current relationship was decreased by increasing [Mg2+]i. Under these conditions, the voltage dependence of IK was not affected. 5. The rate of activation of the current at +40 mV was slowed by increasing [Mg2+]i with little effect on the rate of deactivation at ‐50 mV. This is in contrast to the effects of isoprenaline, which speeded activation and slowed deactivation. 6. Isoprenaline increased IK on average by about 2.5 pA/pF, whether IK had previously run down or not, and regardless of [Mg2+]i. The reversibility of isoprenaline was partially inhibited at [Mg2+]i less than 1 mM. 7. It is concluded that Mg2+ affects IK via several mechanisms that might include a Mg(2+)‐dependent phosphatase.